Autophagy reportsPub Date : 2024-09-04eCollection Date: 2024-01-01DOI: 10.1080/27694127.2024.2396696
Jinying Yang, Limin Shi, Anna L Cubito, James F Collins, Zhiyong Cheng
{"title":"A liver-fat crosstalk for iron flux during healthy beiging of adipose tissue.","authors":"Jinying Yang, Limin Shi, Anna L Cubito, James F Collins, Zhiyong Cheng","doi":"10.1080/27694127.2024.2396696","DOIUrl":"10.1080/27694127.2024.2396696","url":null,"abstract":"<p><p>Beiging of adipocytes is characteristic of a higher number of mitochondria, the central hub of metabolism in the cell. However, studies show that beiging can improve metabolic health or cause metabolic disorders. Here we discuss a liver-fat crosstalk for iron flux associated with healthy beiging of adipocytes. Deletion of the transcription factor FoxO1 in adipocytes (adO1KO mice) induces a higher iron flux from the liver to white adipose tissue, concurrent with augmented mitochondrial biogenesis that increases iron demands. In addition, adO1KO mice adopt an alternate mechanism to sustain mitophagy, which enhances mitochondrial quality control, thereby improving mitochondrial respiratory capacity and metabolic health. However, the liver-fat crosstalk is not detectable in adipose Atg7 knockout (ad7KO) mice, which undergo beiging of adipocytes but have metabolic dysregulation. Autophagic clearance of mitochondria is blocked in ad7KO mice, which accumulates dysfunctional mitochondria and elevates mitochondrial content but lowers mitochondrial respiratory capacity. Mitochondrial biogenesis is comparable in the control and ad7KO mice, and the iron influx into adipocytes and iron efflux from the liver remain unchanged. Therefore, activation of the liver-fat crosstalk is critical for mitochondrial quality control that underlies healthy beiging of adipocytes.</p>","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2396696"},"PeriodicalIF":0.0,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Re-exploration of all <i>ATG</i> genes.","authors":"Kentaro Furukawa, Tamara Ginevskaia, Tomotake Kanki","doi":"10.1080/27694127.2024.2386194","DOIUrl":"10.1080/27694127.2024.2386194","url":null,"abstract":"<p><p>Most autophagy-related (<i>ATG</i>) genes have been identified and characterized through studies using the budding yeast <i>Saccharomyces cerevisiae</i>. However, there are no studies that comprehensively compare the contribution of each <i>ATG</i> gene to non-selective bulk autophagy and various types of selective autophagy, including the cytoplasm-to-vacuole targeting (Cvt) pathway, mitophagy, reticulophagy, and pexophagy. Our recent study quantified these types of autophagy in all <i>atg</i> mutants and showed that (i) autophagy is not completely impaired in specific deletants such as lacking the components of the two ubiquitin conjugation-like (UBL) systems, traditionally regarded as essential for autophagy in yeast, and (ii) residual autophagic activity is especially prominent in mutants of the Atg8 UBL system, which display small autophagic body-like vesicles at a low frequency. Alongside these findings, our comprehensive analysis suggested a link between mitophagy and pexophagy, and a differential contribution of Atg proteins to cargo specificity. We discuss how our datasets are useful for future autophagy research. <b>Abbreviations:</b> Ape1: aminopeptidase I; ATG: autophagy related; Cvt: cytoplasm-to-vacuole targeting; ER: endoplasmic reticulum; ESCRT: endosomal sorting complex required for transport; GFP: green fluorescent protein; PI3K: phosphatidylinositol 3-kinase; UBL: ubiquitin conjugation-like.</p>","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2386194"},"PeriodicalIF":0.0,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}